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Endo > Pituitary Gland > Flashcards

Pituitary Gland Flashcards

1
Q

Order of hormones affected in hypopituitarism

A 
GH
Gonadotropins (FSH + LH)
TSH
ACTH
Prolactin
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2
Q

Hypopituitarism causes

A

Hypothalamic - Kallman’s, tumour, inflammation, infection (meningitis/TB), ischaemia
Pituitary stalk - trauma, mass lesion, carotid artery aneurysm
Pituitary - Tumour, irradiation, inflammation, autoimmune, infiltration (haemochromatosis, amyloid, metastases), ischaemia

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3
Q

Hypopituitarism tests

A

Test hormones secreted and downstream hormones if necessary e.g. T4 for TSH
IGF-1 for GH axis measurement

Short Synthacten test for adrenal axis
Insulin tolerance test (CI: epilepsy, heart disease, adrenal failure)
Glucagon stimulation test if ITT CI
Arginine + GH test

MRI for hypothalamic/ pituitary lesion

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4
Q

What is insulin tolerance test

A

IV insulin given to induce hypoglycaemia in morning (water only from 22:00 night before), cortisol inc and GH secretion normally triggered
Glucose must fall below 2.2mmol/L
Normally GH>20mU/L and peak cortisol >550nmol/L

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5
Q

Hypopituitarism treatment

A

Hydrocortisone for 2˚ adrenal failure

Thyroxine if hypothyroid

Hypogonadism: Testosterone (enanthate IM 250mg every 3wks) in men and oestrogen in premenopausal women
Gonadotropin therapy needed for fertility

Somatotrophin mimics human GH

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6
Q

Pituitary tumour histological types

A

Chromophobe (70%) - Many non-secretory, half produce prolactin, few produce ACTH/GH; local pressure effect in 30%
Acidophil (15%) - Secrete GH or prolactin; local pressure effect in 10%
Basolphil (15%) - Secrete ACTH; local pressure effect rare

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7
Q

Pituitary local pressure effects

A

Headache

Visual field defect
CNIII, IV, VI palsy

Diabetes insipidus
Hypothalamic disturbances to temp, sleep + appetite

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8
Q

Pituitary tumour tests

A

MRI for intra-/supra-sellar extension

Visual field tests

Screening tests: Prolactin, IGF-1, ACTH, cortisol, TFTs, LH/FSH, testosterone in men, short Synthacten test

Glucose tolerance test if acromegaly suspected
Water deprivation if DI suspected

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9
Q

Pituitary tumour treatment

A

Trans-sphenoidal surgery unless supra-sellar extension then trans-frontal, with pre-op 100mg IV/IM hydrocortisone
Radiotherapy for residual/recurrent adenomas

HRT as needed
Steroids before levothyroxine as thyroxine may cause adrenal crisis
If prolactinoma then dopamine agonist 1st line

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10
Q

What is pituitary apoplexy

A

Rapid pituitary enlargement from bleed into tumour

Can cause mass effects, CV collapse due to acute hypopituitarism

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11
Q

When to suspect pituitary apoplexy

A 
All acute:
GCS drop
Headache
Meningism
Opthalmoplegia
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12
Q

Pituitary apoplexy treatment

A

Hydrocortisone 100mg IV
Fluid balance very well controlled
±cabergoline (dopamine agonist) if prolactinoma
± surgery
Find cause e.g. predisposition to thrombosis from antiphospholipid syndrome

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13
Q

What is a craniopharyngioma

A

Situated between pituitary and 3rd ventricle floor

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14
Q

Craniopharyngioma presentation

A

Over 50% in childhood with growth failure

In adults amenorrhea, dec libido, hypothalamic symptoms, tumour mass effect e.g. visual field

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15
Q

Craniopharyngioma tests

A

CT/MRI (calcification in 50% so may be seen on skull XR)

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16
Q

Craniopharyngioma treatment

A

Surgery ± post-op radiation

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17
Q

Prolactin physiology

A

Secreted by anterior pituitary

Release inhibited by dopamine produced in hypothalamus

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18
Q

Hyperprolactinaemia causes

A

Excess production (e.g. prolactinoma)
Disinhibition through pituitary stalk compression
Dopamine antagonist use (antipsychotics, MDMA, oestrogens, metoclopramide, haloperidol, methyldopa)
Pregnancy/ breastfeeding/ stress
Hypothyroidism (due to inc TRH)
Chronic renal failure (dec excretion)

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19
Q

Hyperprolactinaemia presentation

A 
Menstrual disturbance in women
ED/mass effects in men
Hypogonadism
Osteoporosis
Galactorrhoea
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20
Q

Hyperprolactinaemia tests

A 
Basal prolactin (non-stressful venepuncture between 9-16h)
Pregnancy test
TFT
U+Es
MRI pituitary if other causes ruled out
21
Q

Hyperprolactinaemia management

A 
Refer to endo
Dopamine agonists (bromocriptine/ cabergoline) 1st line
22
Q

Microprolactinoma (<10mm) management

A

Bromocriptine 1.25mg PO titrated up weekly by 1.25mg/d until ~2.5mg/12h
Cabergoline is alternative but safety unknown in pregnancy
Trans-sphenoidal surgery 2nd line due to reoccurence and hormone deficiency risks

23
Q

Macroprolactinoma (>10mm) management

A

Bromocriptine if fertility needed
Surgery followed by bromocriptine ± radiation post op, if visual symptoms or pressure effects unmanageable medically
Monitor closely if medical

24
Q

Hyperprolactinaemia follow up

A

Monitor PRL, check for headaches/visual field loss

Medication can be decreased after 2yrs with monitoring

25
Q

What is acromegaly

A

Phenotype of increased GH, 99% due to pituitary tumour

GH stimulates bone and soft tissue growth via secretion of IGF-1

26
Q

Acromegaly presentation

A 
Acroparasthesia (acro= extremities)
Amenorrhoea
Inc sweating + snoring
Arthralgia + backache
Acanthosis nigricans
Large jaw, face, nose, hands and feet
Proximal weakness + arthropathy
Carpal tunnel signs in 50%
27
Q

Acromegaly complications

A

Impaired glucose tolerance (40%), DM (~15%)
Vascular - HT, LVH, arrythmias, inc IHD + stroke risk
Neoplasia - colon ca risk

28
Q

Acromegaly in pregnancy

A

Pregnancy may be normal, signs and chemistry may remit

29
Q

Acromegaly tests

A

Raised glucose, Ca and PO4

If basal GH >0.4mcg/L and/or IGF-1 raised then OGTT, then if OGTT >1mcg/L (glucose normally suppresses GH) then acromegaly confirmed

MRI of pituitary fossa
Look for hypopituitarism
Visual fields/acuity

ECG/echo
Old photos

30
Q

OGTT in acromegaly testing

A

Collect samples for GH glucose every 30 mins from 0-150

False +ves from puberty, pregnancy, hepatic/renal disease, anorexia nervosa and DM

31
Q

Acromegaly treatment

A

Trans-sphenoidal surgery 1st line
Radiotherapy if unsuitable for surgery or as adjuvant

Somatostatin analogues (octreotide/lanreotide IM) if surgery fails

GH antagonist pegvisomant if SSA not an option, suppresses IGF-1 to normal in 90% but GH levels may rise

32
Q

Acromegaly treatment follow up

A 
Yearly:
GH, IGF-1 and OGTT
Visual fields
Vasc assessment
BMI
Photos
33
Q

Acromegaly prognosis

A

May return to normal, excess mortality mostly vasc complications
16% get diabetes with SSAs, 13% after surgery

34
Q

What is diabetes insipidus

A

Passing lots of dilute urine (>3L/d) due to impaired water reabsorption in kidney from low ADH secretion (cranial DI) or impaired response to ADH (nephrogenic DI)

35
Q

Diabetes insipidus symptoms

A

Polyuria/dipsia
Dehydration
HyperNa symptoms

36
Q

Cranial DI causes

A

50% idiopathic
Congenital - DIDMOAD, ADH defects
Tumour - craniopharyngioma, metastases, pituitary
Trauma - temporary if distal to pituitary stalk
Hypophysitis/ectomy
Infiltration - sarcoidosis, histiocytosis
Haemorrhage
Meningoencephalitis

37
Q

What is DIDMOAD

A

DI, DM, Optic atrophy, deafness
Rare autosomal recessive disorder
Also known as Wolfram’s syndrome

38
Q

Nephrogenic DI causes

A 
Inherited
Metabolic - low K, high Ca
Drugs - Lithium, demeclocycline
Chronic renal disease
Post-obstructive uropathy
39
Q

Diabetes insipidus tests

A

Glucose (exclude DM)
U+E
Serum (285-295mOsmol/kg normally) + urine (2x serum) osmolalities
Diagnose with water deprivation tests, primary polydipsia is a differential with hypoNa

40
Q

Cranial DI treatment

A 
MRI head, test anterior pituitary function
Give desmopressin (ADH analogue)
41
Q

Nephrogenic DI treatment

A

Treat cause
Bendroflumethiazide 5mg/24h PO if persists
NSAIDs lower urine volume and plasma Na by inhibiting prostaglandin synthase (prostaglandins locally inhibit ADH action)

42
Q

Diabetes insipidus emergency management

A

Urgent plasma U+Es and serum + urine osmolalities
IVI to keep up with urine output, use 0.9% saline initially
Lower Na slowly (lower <12mmol/L per day), any faster may cause cerebral oedema + brain injury
Desmopressin 2mcg IM (lasts 12-24h) may be used as therapeutic trial

43
Q

8hr water deprivation test when to do it

A

When established that urine output >3L/d

44
Q

8hr water deprivation test preparation

A

Free fluids until 7.30, light breakfast at 6.30 if starting at 8.00
No tea, coffee or smoking

45
Q

8hr water deprivation test stage 1

A

Fluid deprivation start at 8.00
Empty bladder then no drinks, just dry food
Weigh hourly, if >3% weight lost or serum osmolality rises>300mOsmol/kg go to stage 2, if less continue stage 1
Collect urine every 2h, measure osmolality and volume
Venous osmolality sample every 4h
Stop test after 8h if urine osmolality >600 (normal)

46
Q

8hr water deprivation test stage 2

A

Distinguish between nephrogenic + cranial
Give desmopressin 2mcg IM, can drink water now
Measure urine osmolality hourly for 4h

47
Q

8hr water deprivation test urine osmolality result interpretations

A

If normal, urine:plasma osmolality ratio >2
If 1˚ polydipsia, urine concentrates but less than normal e.g. >400-600mOsmol/kg
If cranial DI, urine osmolality increase >600 after desmopressin, if ambiguous then extended water deprivation test (from 18.00 night before, no water)
If nephrogenic DI, no inc in urine osmolality after desmopressin

48
Q

What is SIADH

A

Syndrome of inappropriate ADH secretion, even when low plasma osmolality/ large plasma volume

49
Q

SIADH diagnosis

A

Concentrated urine (Na>20mmol/L and Na osmolality >100mOsmol/kg) with hyponatraemia and low plasma osmolality

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